Pancreatic cancer is among the most aggressive cancer types, with survival rates being very low and current treatment being quite ineffective. To address this unmet medical need, HCW Biologics Inc. has developed and presented preclinical data for their T-cell engager approach – HCW11-018.
Université de Montréal has identified compounds acting as proto-oncogene tyrosine-protein kinase Src (SRC; SRC1) and/or tyrosine-protein kinase Yes (YES1) inhibitors reported to be useful for the treatment of cancer, fibrosis and liver diseases.
Hutchmed Ltd. has identified antibody-drug conjugates comprising an antibody or antigen binding fragment covalently linked to a GTPase RAS or KRAS inhibitor through a linker reported to be useful for the treatment of cancer.
Adlai Nortye Biopharma Co. Ltd. and Adlai Nortye Pte Ltd. have divulged GTPase KRAS (mutant) inhibitors reported to be useful for the treatment of cancer, inflammatory diseases and immunological disorders.
Although tricomplex pan-RAS (ON) inhibitors, such as RMC-6236, constitute a promising class of therapeutics against RAS-driven cancers, their on-target, off-tumor toxicities challenge the dosing strategy and the safety of drug combinations.
Pinotbio Inc. recently reported a novel antibody-drug conjugate (ADC), named PBX-004, consisting of an ITGB6-targeting antibody conjugated to a potent topoisomerase I (TOP1) inhibitor payload.
Shanghai Leadingtac Pharmaceutical Co. Ltd. has synthesized proteolysis targeting chimera (PROTAC) compounds comprising an E3 ubiquitin ligase-binding moiety covalently linked to a GTPase KRAS (G12D mutant)-targeting moiety via a linker reported to be useful for the treatment of cancer.
A team from the University of Missouri and collaborating institutions aimed to investigate the role of ABTB2 expression in pancreatic ductal adenocarcinoma cells. To do that, they applied a comprehensive suite of functional genomics tools, including siRNA/shRNA knockdown, CRISPR-Cas9 knockout, plasmid-based overexpression and a Cre-LoxP transgenic mouse model to modulate ABTB2 expression.
